Evidence map›Paper›PMID 37038107›Full record

ArticleMolecular medicine (Cambridge, Mass.)2023

Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infection.

Uzma Khan, Bipul Chandra Karmakar, Priyanka Basak, Sangita Paul, Animesh Gope, Deotima Sarkar, Asish Kumar Mukhopadhyay, Shanta Dutta, Sushmita Bhattacharya

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 21 citations in OpenAlex.

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  7. Research Status and Prospects ofGastroenterology research and practice · 2026
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  8. Polyphenolic compounds inFrontiers in pharmacology · 2026
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  14. Review
  15. Article
  16. Programmed cell death inFrontiers in cellular and infection microbiology · 2024
    Review
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Uzma KhanDivision of Biochemistry ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Bipul Chandra KarmakarDivision of Bacteriology ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Priyanka BasakDivision of Biochemistry ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Sangita PaulDivision of Bacteriology ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Animesh GopeDivision of Clinical Medicine, ICMR-NICED, ICMR- National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, India.
Deotima SarkarDivision of Biochemistry ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Asish Kumar MukhopadhyayDivision of Bacteriology ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Shanta DuttaDivision of Bacteriology ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India.
Sushmita BhattacharyaDivision of Biochemistry ICMR-NICED, ICMR-National Institute of Cholera and Enteric Diseases (ICMR-NICED), Kolkata, 700010, India. durgasushmita@gmail.com.ORCID 0000-0001-8437-4197
National Institute of Cholera and Enteric Diseases · IN

Funding

Department of Biotechnology, Ministry of Science and Technology, India BT/PR3093/BIC/101/1076/2018
6 · The paper itself

Abstract

backgroundHelicobacter pylori is a key agent for causing gastric complications linked with gastric disorders. In response to infection, host cells stimulate autophagy to maintain cellular homeostasis. However, H. pylori have evolved the ability to usurp the host's autophagic machinery. High mobility group box1 (HMGB1), an alarmin molecule is a regulator of autophagy and its expression is augmented during infection and gastric cancer. Therefore, this study aims to explore the role of glycyrrhizin (a known inhibitor of HMGB1) in autophagy during H. pylori infection. MAIN

methodsHuman gastric cancer (AGS) cells were infected with the H. pylori SS1 strain and further treatment was done with glycyrrhizin. Western blot was used to examine the expression of autophagy proteins. Autophagy and lysosomal activity were monitored by fluorescence assays. A knockdown of HMGB1 was performed to verify the effect of glycyrrhizin. H. pylori infection in in vivo mice model was established and the effect of glycyrrhizin treatment was studied.

resultsThe autophagy-lysosomal pathway was impaired due to an increase in lysosomal membrane permeabilization during H. pylori infection in AGS cells. Subsequently, glycyrrhizin treatment restored the lysosomal membrane integrity. The recovered lysosomal function enhanced autolysosome formation and concomitantly attenuated the intracellular H. pylori growth by eliminating the pathogenic niche. Additionally, glycyrrhizin treatment inhibited inflammation and improved gastric tissue damage in mice.

conclusionThis study showed that inhibiting HMGB1 restored lysosomal activity to ameliorate H. pylori infection. It also demonstrated the potential of glycyrrhizin as an antibacterial agent to address the problem of antimicrobial resistance.

Indexed as

Helicobacter InfectionsHelicobacter pyloriHMGB1 ProteinStomach NeoplasmsAnimalsAutophagyGlycyrrhizic AcidHumansMiceGlycyrrhizic AcidHMGB1 ProteinAutophagyGlycyrrhizinHelicobacter pyloriHMGB1LMP

Identifiers

PMID37038107
PMCPMC10088177
OpenAlexW4363675929

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.